Circadian Effects on Attention and Working Memory in College Students With Attention Deficit and Hyperactivity Symptoms.

Objective: Individuals with an evening chronotype prefer to sleep later at night, wake up later in the day and perform best later in the day as compared to individuals with morning chronotype. Thus, college students without ADHD symptoms with evening chronotypes show reduced cognitive performance in the morning relative to nighttime (i.e., desynchrony effect). In combination with symptoms presented in attention deficit hyperactivity disorder (ADHD), we predicted that having evening chronotype renders impairment in attention during the morning, when students require optimal performance, amplifying desynchrony. Method: Four hundred college students were surveyed for evening chronotype and symptoms of ADHD. Of those surveyed, 43 students with evening chronotype (19 with ADHD symptoms) performed laboratory attention tasks and were queried about fatigue during morning and evening sessions. Results: Students with ADHD symptoms demonstrated a greater decrement in sustained attentional vigilance when abstaining from stimulants and asked to perform cognitive tests at times misaligned with natural circadian rhythms in arousal compared to their non-ADHD counterparts with the same chronotype. While individuals with ADHD symptoms had slower reaction-times during sustained attention tasks in the morning session compared to those without symptoms, there was no significant group difference in working memory performance, even though both groups made more errors in the morning session compared to the evening session. Conclusion: These findings suggest that evening chronotype students with ADHD symptoms are at a greater disadvantage when having to perform sustained attention tasks at times that are not aligned to their circadian rhythm compared to their neuro-typical peers. The implications of this finding may be useful for the provision of disability accommodations to college age students with ADHD when they are expected to perform tasks requiring sustained attention at times misaligned with their circadian rhythms.

Early Life Trauma Has Lifelong Consequences for Sleep And Behavior.

Sleep quality varies widely across individuals, especially during normal aging, with impaired sleep contributing to deficits in cognition and emotional regulation. Sleep can also be impacted by a variety of adverse events, including childhood adversity. Here we examined how early life adverse events impacted later life sleep structure and physiology using an animal model to test the relationship between early life adversity and sleep quality across the life span. Rat pups were exposed to an Adversity-Scarcity model from postnatal day 8-12, where insufficient bedding for nest building induces maternal maltreatment of pups. Polysomnography and sleep physiology were assessed in weaning, early adult and older adults. Early life adversity induced age-dependent disruptions in sleep and behavior, including lifelong spindle decreases and later life NREM sleep fragmentation. Given the importance of sleep in cognitive and emotional functions, these results highlight an important factor driving variation in sleep, cognition and emotion throughout the lifespan that suggest age-appropriate and trauma informed treatment of sleep problems.

Sleep oscillation-specific associations with Alzheimer's disease CSF biomarkers: novel roles for sleep spindles and tau.

BACKGROUND: Based on associations between sleep spindles, cognition, and sleep-dependent memory processing, here we evaluated potential relationships between levels of CSF Aß42, P-tau, and T-tau with sleep spindle density and other biophysical properties of sleep spindles in a sample of cognitively normal elderly individuals. METHODS: One-night in-lab nocturnal polysomnography (NPSG) and morning to early afternoon CSF collection were performed to measure CSF Aß42, P-tau and T-tau. Seven days of actigraphy were collected to assess habitual total sleep time. RESULTS: Spindle density during NREM stage 2 (N2) sleep was negatively correlated with CSF Aß42, P-tau and T-tau. From the three, CSF T-tau was the most significantly associated with spindle density, after adjusting for age, sex and ApoE4. Spindle duration, count and fast spindle density were also negatively correlated with T-tau levels. Sleep duration and other measures of sleep quality were not correlated with spindle characteristics and did not modify the associations between sleep spindle characteristics and the CSF biomarkers of AD. CONCLUSIONS: Reduced spindles during N2 sleep may represent an early dysfunction related to tau, possibly reflecting axonal damage or altered neuronal tau secretion, rendering it a potentially novel biomarker for early neuronal dysfunction. Given their putative role in memory consolidation and neuroplasticity, sleep spindles may represent a mechanism by which tau impairs memory consolidation, as well as a possible target for therapeutic interventions in cognitive decline.